Abstract

Aggregation of LDL is considered the initial key event in atherogenesis and apoJ is an extracellular chaperone part of the quality control system against protein aggregation. A minor fraction of apoJ in blood is transported by LDL, but its role is poorly understood. Considering both the importance of LDL aggregation in atherosclerosis and the modulatory role of apoJ on protein aggregation, the function of apoJ bound to LDL could be relevant. Recent studies have shown that apoJ prevents the LDL aggregation and inhibits the cytotoxic potential of modified LDL. Other studies have reported increased content of apoJ in atherogenic LDL fractions. These observations point to apoJ as a key modulator of LDL atherogenicity.

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